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Background: Social cognitive difficulties in Autism Spectrum Disorder (ASD) can affect the daily lives of people with ASD profoundly, impacting the development and maintenance of meaningful social relations. Social cognition training (SCT) is commonly used for improving social functioning, but lacks ecological validity and the ability to effectively mimic social situations. Development of virtual reality (VR) interventions, focusing on enhancing social cognition, could add to the effectiveness of SCT within ASD care, by offering a safe, interactive and practical training setting, where generalization of knowledge and skills to the real-world are promoted. In this paper, our primary aim is to evaluate the feasibility and acceptance by participants and therapists of the Dynamic Interactive Social Cognition Method: Training in Virtual Reality (DiSCoVR) protocol as developed for adults with schizophrenic spectrum disorder (SSD), adapted for ASD (DiSCoVR-A). 26 participants, aged 18–63, took part in a pilot study. 22 participants completed baseline and post-assessment, including primary outcome evaluation assessment through a semi-structured interview. Secondary measures focused on social cognition, emotion recognition, mental flexibility, social anxiety, empathy and social responsiveness and were assessed at baseline (T0), post-treatment (T1), and at follow-up (T2) sixteen weeks after completion of the intervention. Results: Our results show that the majority of participant and therapists found the VR intervention acceptable and feasible, as reported in evaluation questionnaires and interviews. Conclusion: These preliminary findings are promising; however, controlled research is needed to further investigate the effectiveness of VR within social cognition training for adults with ASD.

Objective: Metabolic syndrome (MS) is highly prevalent in schizophrenia and often a consequence of unhealthy behaviour. Reward-related brain areas might be associated with MS, since they play a major role in regulating health behaviour. This study examined the relationship between MS and brain volumes related to the reward system in schizophrenia. Method: We included patients with schizophrenia, with MS (MS+; n = 23), patients with schizophrenia, without MS (MS; n = 48), and healthy controls (n = 54). Global brain volumes and volumes of (sub)cortical areas, part of the reward circuit, were compared between patients and controls. In case of a significant brain volume difference between patients and controls, the impact of MS in schizophrenia was examined. Results: Patients had smaller total brain (TB; P = 0.001), GM (P = 0.010), larger ventricles (P = 0.026), and smaller reward circuit volume (P < 0.001) than controls. MS+ had smaller TB (P = 0.017), GM (P = 0.008), larger ventricles (P = 0.015), and smaller reward circuit volume (P = 0.002) than MS. MS+ had smaller orbitofrontal cortex (OFC; P = 0.002) and insula volumes (P = 0.005) and smaller OFC (P = 0.008) and insula cortical surface area (P = 0.025) compared to MS. Conclusion: In schizophrenia, structural brain volume reductions in areas of the reward circuitry appear to be related to comorbid MS.

Subcortical brain structures are integral to motion, consciousness, emotions and learning. We identified common genetic variation related to the volumes of the nucleus accumbens, amygdala, brainstem, caudate nucleus, globus pallidus, putamen and thalamus, using genome-wide association analyses in almost 40,000 individuals from CHARGE, ENIGMA and UK Biobank. We show that variability in subcortical volumes is heritable, and identify 48 significantly associated loci (40 novel at the time of analysis). Annotation of these loci by utilizing gene expression, methylation and neuropathological data identified 199 genes putatively implicated in neurodevelopment, synaptic signaling, axonal transport, apoptosis, inflammation/infection and susceptibility to neurological disorders. This set of genes is significantly enriched for Drosophila orthologs associated with neurodevelopmental phenotypes, suggesting evolutionarily conserved mechanisms. Our findings uncover novel biology and potential drug targets underlying brain development and disease.

BackgroundLower intelligence quotient (IQ) has frequently been reported in patients with schizophrenia. However, it is unclear whether IQ declines (further) after illness onset and what the familial contribution is to this change. Therefore, we investigate IQ changes during the course of illness in patients with non-affective psychosis, their siblings and controls.MethodsData are part of the longitudinal Genetic Risk and Outcome of Psychosis (GROUP) study in the Netherlands and Belgium. Participants underwent three measurements, each approximately 3 years apart. A total of 1022 patients with non-affective psychosis [illness duration: 4.34 (s.d.= 4.50) years], 977 of their siblings, and 565 controls had at least one measure of IQ (estimated from four subtests of the WAIS-III).ResultsAt baseline, IQ was significantly lower in patients (IQ = 97.8) and siblings (IQ = 108.2;p< 0.0001) than in controls (IQ = 113.0;p< 0.0001), and in patients as compared with siblings (p< 0.0001). Over time, IQ increased in all groups. In siblings, improvement in IQ was significantly more pronounced (+0.7 points/year) than in patients (+0.5 points/year;p< 0.0001) and controls (+0.3 points/year;p< 0.0001). IQ increase was not significantly correlated with improvement in (sub)clinical outcome in any of the groups.ConclusionsDuring the first 10 years of the illness, IQ increases to a similar (and subtle) extent in a relatively high-functioning group of schizophrenia patients and controls, despite the lower IQ in patients at baseline. In addition, the siblings’ IQ was intermediate at baseline, but over time the increase in IQ was more pronounced.

Obsessive–compulsive symptoms (OCS) are frequently reported in patients with schizophrenia and have been associated with subjective distress and higher impairment. Recent studies suggest fluctuation in co-occurring OCS and associations with the course of psychotic symptoms. Current evidence is limited by few studies with long assessments intervals and a sole focus on between-subject comparisons. The aim of this study was to specifically investigate co-variation of symptom domains over time within individuals. Patients with a psychotic disorder (n = 56) and un-affected siblings (n = 49) completed monthly assessments of clinical and subclinical symptoms over 6 months. Mixed-model multilevel analyses examined the variability and relationship between OCS and positive, negative, and depressive symptoms on the between- and within-subject level. Symptom domains were associated across subjects and assessment times, in patients and siblings, with the strongest association between OCS and (subclinical) positive symptoms. Within-subjects, substantial variability and co-variation of all symptom domains was found. Particularly, between-subject differences in positive symptoms and within-subject change in depressive symptoms predicted subsequent OCS in patients 1 months later. This is the first prospective study disaggregating between and within-subject associations between co-occurring OCS and symptom cluster of psychosis. Differences on these two levels suggest different underlying mechanisms. The association between depressive symptoms and subsequent increase/decrease of OCS within patients may have important treatment implications. Electronic supplementary material The online version of this article (10.1007/s00406-018-0884-4) contains supplementary material, which is available to authorized users.

Subcortical brain structures are integral to motion, consciousness, emotions and learning. We identified common genetic variation related to the volumes of the nucleus accumbens, amygdala, brainstem, caudate nucleus, globus pallidus, putamen and thalamus, using genome-wide association analyses in almost 40,000 individuals from CHARGE, ENIGMA and UK Biobank. We show that variability in subcortical volumes is heritable, and identify 48 significantly associated loci (40 novel at the time of analysis). Annotation of these loci by utilizing gene expression, methylation and neuropathological data identified 199 genes putatively implicated in neurodevelopment, synaptic signaling, axonal transport, apoptosis, inflammation/infection and susceptibility to neurological disorders. This set of genes is significantly enriched for Drosophila orthologs associated with neurodevelopmental phenotypes, suggesting evolutionarily conserved mechanisms. Our findings uncover novel biology and potential drug targets underlying brain development and disease.

BackgroundA range of endophenotypes characterise psychosis, however there has been limited work understanding if and how they are inter-related.MethodsThis multi-centre study includes 8754 participants: 2212 people with a psychotic disorder, 1487 unaffected relatives of probands, and 5055 healthy controls. We investigated cognition [digit span (N= 3127), block design (N= 5491), and the Rey Auditory Verbal Learning Test (N= 3543)], electrophysiology [P300 amplitude and latency (N= 1102)], and neuroanatomy [lateral ventricular volume (N= 1721)]. We used linear regression to assess the interrelationships between endophenotypes.ResultsThe P300 amplitude and latency were not associated (regression coef. −0.06, 95% CI −0.12 to 0.01,p= 0.060), and P300 amplitude was positively associated with block design (coef. 0.19, 95% CI 0.10–0.28,p< 0.001). There was no evidence of associations between lateral ventricular volume and the other measures (allp> 0.38). All the cognitive endophenotypes were associated with each other in the expected directions (allp< 0.001). Lastly, the relationships between pairs of endophenotypes were consistent in all three participant groups, differing for some of the cognitive pairings only in the strengths of the relationships.ConclusionsThe P300 amplitude and latency are independent endophenotypes; the former indexing spatial visualisation and working memory, and the latter is hypothesised to index basic processing speed. Individuals with psychotic illnesses, their unaffected relatives, and healthy controls all show similar patterns of associations between endophenotypes, endorsing the theory of a continuum of psychosis liability across the population.

Background Multimorbidity may impose an overwhelming burden on patients with psychosis and is affected by gender and age. Our aim is to study the independent role of familial liability to psychosis as a risk factor for multimorbidity. Methods We performed the study within the framework of the Genetic Risk and Outcome of Psychosis (GROUP) project. Overall, we compared 1024 psychotic patients, 994 unaffected siblings and 566 controls on the prevalence of 125 lifetime diseases, and 19 self-reported somatic complaints. Multimorbidity was defined as the presence of two or more complaints/diseases in the same individual. Generalized linear mixed model (GLMM) were used to investigate the effects of gender, age (adolescent, young, older) and familial liability (patients, siblings, controls) and their interactions on multimorbidity. Results Familial liability had a significant effect on multimorbidity of either complaints or diseases. Patients had a higher prevalence of multimorbidity of complaints compared to siblings (OR 2.20, 95% CI 1.79–2.69, P

Background Patients with schizophrenia suffer from fundamental self-disturbances and have difficulties integrating and distinguishing between the self and others. For example, they experience that bodily boundaries vanish, that body parts are located at the wrong part of the body or that they are not the subject of their own movements. Such experiences are referred to as disturbances in the sense of body ownership. Although these are well-described psychotic symptoms, surprisingly little is known about their etiology and development. Our aim was to replicate a more flexible sense of body ownership in patients, thereby using a well-controlled experimental procedure (with proprioceptive drift and subjective strength of the illusion. Second, we examine whether increased familial risk to develop psychosis (i.e., offspring of patients with schizophrenia), relative to increased familial risk to develop mood disorders or the absence of familial risk, is related to alterations in RHI measures. Methods With a Rubber Hand Illusion (RHI) paradigm, body ownership was assessed in two different cohorts: 1) 54 patients with schizophrenia and 56 age and gender matched controls and 2) 24 children/adolescents with at least one parent with schizophrenia, 33 children/adolescents with at least one parent with bipolar disorder, and 18 age and gender matched controls. In this paradigm, a visible rubber hand and the invisible real hand were stroked either synchronously or asynchronously. Subsequently, proprioceptive drift and subjective RHI were measured. Results All groups showed the rubber hand illusion, i.e., a stronger proprioceptive drift and higher subjective ratings of the RHI after synchronous compared with asynchronous stroking (all p

Schizophrenia is a severe mental disorder striking mainly young adults and leading to life-long disability in a substantial portion of the sufferers. On the other hand, substantial knowledge about its etiology and pathogenesis is still lacking. Therefore the European Science Foundation (ESF) sponsored a meeting of a panel of European experts on schizophrenia research to discuss the state of art and future perspectives of key topics in this area. The fields covered genetics, epidemiology, animal models, molecular neuropathology and imaging. This was a first step to establish a network of European groups dedicated to Schizophrenia research. The coming calls of the frame work program will be used to strengthen this network in order to achieve substantial progress in understanding and treating this devastating illness. © 2008.